atrial-natriuretic-factor and Hypopituitarism

Adrenomedullin, a 52-amino acid residue peptide, has numerous biological actions which are of potential importance to cardiovascular homeostasis, growth and development of cardiovascular tissues and bone, prevention of infection, and regulation of body fluid and electrolyte balance. Studies in man using intravenous infusion of the peptide have demonstrated that, at plasma levels detected after myocardial infarction or in heart failure, adrenomedullin reduces arterial pressure, increases heart rate and cardiac output, and activates the sympathetic and renin-angiotensin systems but suppresses aldosterone. The thresholds for these responses differ, being lower under some experimental circumstances for arterial pressure than for the other biological effects. Adrenomedullin administration inhibits the pressor and aldosterone-stimulating action of angiotensin II in man. By contrast, the pressor effect of norepinephrine is little altered by concomitant adrenomedullin administration. Although in the absence of a safe, specific antagonist of the actions of endogenous adrenomedullin it is difficult to be certain about the physiological and pathophysiological importance of this peptide in man, current evidence suggests that it serves to protect against cardiovascular overload and injury. Hope has been expressed that adrenomedullin or an agonist specific for adrenomedullin receptors might find a place in the treatment of cardiovascular disorders.

Topics: Adrenomedullin; Animals; Atrial Natriuretic Factor; Blood Pressure; Cardiotonic Agents; Endothelins; Heart Failure; Heart Rate; Hemodynamics; Humans; Hypertension; Hypopituitarism; Peptides

Symptoms of fluid retention in GH-deficient patients during GH replacement are greater in men than in women, suggesting that testosterone may augment or estradiol may attenuate the antinatriuretic actions of GH. The mechanisms underlying the sodium-retaining effects of GH are poorly understood.. The aim of this study was to investigate the effects of GH and testosterone, alone and in combination, on extracellular water (ECW) and the hormonal mechanisms involved.. Two separate, open-label, randomized, two-period, crossover studies were performed; the first compared the effects of GH alone with those of GH and testosterone, and the second compared the effects of testosterone alone with those of GH and testosterone.. Twelve hypopituitary men with GH deficiency and hypogonadism were studied.. During the weeks of intervention, GH (0.5 mg/d) and testosterone enanthate (250 mg) were administered by im injection.. The outcome measures were ECW, IGF-I, plasma renin activity (PRA), aldosterone (Aldo), and atrial natriuretic peptide (ANP).. GH treatment significantly increased (P < 0.05) both IGF-I and ECW, and these changes were enhanced by cotreatment with testosterone (P = 0.07 for both). PRA, Aldo, and ANP levels did not change. Testosterone treatment alone did not change the IGF-I concentration, whereas cotreatment with GH induced a marked increase. Testosterone alone increased (P < 0.05) ECW, and the effect was augmented (P < 0.01) by cotreatment with GH. Although PRA and ANP did not change, plasma Aldo decreased after single and combined treatments.. GH and testosterone exerted independent and additive effects on ECW. The mechanisms of fluid retention for both hormones are likely to be exerted on the renal tubules. This is the first direct evidence that testosterone increases ECW.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Body Water; Cross-Over Studies; Drug Synergism; Extracellular Fluid; Hormone Replacement Therapy; Human Growth Hormone; Humans; Hypopituitarism; Insulin-Like Growth Factor I; Male; Middle Aged; Testosterone

Severe adult growth hormone deficiency (AGHD) is associated with increased cardiovascular risk. We have therefore investigated levels of amino terminal pro-brain natriuretic peptide (Nt-proBNP), a well established biomarker for cardiac failure, in adult GHD patients before and after GH replacement therapy, and potential parallel variations in cardiac function. Nt-proBNP concentrations were determined at baseline and after GH treatment in two studies including 28 and 12 patients with severe AGHD, respectively. In the second study, a maximal exercise test and a doppler echocardiography were performed to assess cardiac functional parameters. At baseline, Nt-proBNP levels were higher in AGHD patients than in controls (median: 7.8 vs. 3.7 pmol/L; p < 0.01 in study 1; 8.4 vs. 4.1 pmol/L; p < 0.01 in study 2). Following GH treatment, Nt-proBNP levels decreased significantly in both studies. None of the AGHD patients had signs of cardiac dysfunction at baseline and no significant effect of GH replacement therapy was observed on cardiac functional parameters, independent of changes in Nt-proBNP. In conclusion, GH treatment markedly reduces Nt-proBNP concentrations in adult GHD patients without obvious parallel changes in cardiac functional parameters. These results suggest that Nt-proBNP may appear as a biomarker of GH status and GH treatment efficiency.

Topics: Adult; Analysis of Variance; Atrial Natriuretic Factor; Blood Pressure; Case-Control Studies; Creatinine; Exercise Test; Female; Heart Function Tests; Heart Rate; Hormone Replacement Therapy; Human Growth Hormone; Humans; Hypopituitarism; Insulin-Like Growth Factor I; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Ultrasonography

A 23-year-old man developed acute renal failure (ARF) due to hemorrhagic fever with renal syndrome (HFRS). The patient also developed anterior hypopituitarism as a complication of HFRS. The patient's oliguric phase was very much prolonged for over 10 days before the diuresis began. The urine output during the oliguric phase was near anuric (< 50 ml/day). Interestingly, the patient began to diurese just after the institution of glucocorticoid and thyroid hormone replacement therapy. The plasma atrial natriuretic polypeptide went up to a smaller peak (150.0 pg/ml) at the onset of diuresis compared with 15 other patients (292.4 +/- 190.4 pg/ml) who did not develop anterior hypopituitarism. The delayed onset of diuresis and smaller increase of plasma ANP may have a causal relationship with the patient's hypopituitarism.

Topics: Acute Kidney Injury; Adult; Atrial Natriuretic Factor; Diuresis; Hemorrhagic Fever with Renal Syndrome; Humans; Hypopituitarism; Male; Pituitary Gland, Anterior; Radioimmunoassay; Renin

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism, an acute oral water load of 20 ml.kg-1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N = 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.

Topics: Adult; Aged; Arginine Vasopressin; Atrial Natriuretic Factor; Drinking; Female; Humans; Hydrocortisone; Hypopituitarism; Male; Middle Aged; Osmolar Concentration; Time Factors